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Biomedical subjects

C K Stone

Publications and source records attributed to C K Stone.

At least 73 records · Page 4Linked to original sources
PubMed1989

Effects of pinacidil on myocardial blood flow and infarct size after acute left anterior descending coronary artery occlusion and reperfusion in awake dogs with and without a coexisting left circumflex coronary artery stenosis.

To determine whether partial stenosis of a second major coronary artery promoted vasodilator-induced coronary steal and increased infarct size after acute coronary artery occlusion, we produced acute myocardial infarction by 4-h left anterior descending coronary artery occlusion and 20-h reperfusion in awake dogs with and without a mild to moderate stenosis (33-72%) of the proximal left circumflex coronary artery. Dogs were randomized to receive intravenous (i.v.) normal saline or pinacidil, a new antihypertensive agent with a marked coronary dilator property, beginning 40 min after onset of coronary artery occlusion and continuing throughout the occlusion and the first hour of reperfusion. Pinacidil was titrated to decrease mean aortic pressure 25 mm Hg, which resulted in an increase in heart rate (HR), cardiac output (CO), and left ventricular (LV) dP/dt and LVdP/dt/P. Saline infusion had no effects. Blood flows to ischemic and remote myocardium did not differ between dogs with and without coronary stenosis. Pinacidil increased blood flow threefold in normal myocardium, but had no effect on infarct zone myocardial blood flow or infarct size (58 +/- 4% of region at risk vs. 56 +/- 4% in animals receiving normal saline) in dogs without coronary stenosis. In contrast, similar administration of pinacidil in dogs with coronary stenosis reduced infarct size zone myocardial blood flow and increased infarct size (69 +/- 3% vs. 55 +/- 5% in the saline group, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Opiate receptor antagonism in right-sided congestive heart failure. Naloxone exerts salutary hemodynamic effects through its action on the central nervous system.

Opiate receptor inhibition causes adrenergic receptor-mediated increases in aortic pressure, cardiac output, and left ventricular contractile function in right heart failure. To study whether the effects of opiate receptor inhibition are mediated by means of an action on the central opiate system, we administered equimolar doses of naloxone hydrochloride and naloxone methobromide (MeBr) and normal saline to heart failure dogs. Chronic stable right heart failure was produced by progressive pulmonary artery constriction and tricuspid valve avulsion. Naloxone hydrochloride caused an increase in mean aortic pressure, cardiac output, left ventricular dP/dt and dP/dt/P, plasma catecholamines, and regional blood flows to the myocardium, quadriceps muscle, kidneys, and splanchnic beds. Plasma beta-endorphin and adrenocorticotropin also increased. In contrast, neither normal saline nor naloxone MeBr (which does not cross the blood-brain barrier) affected the systemic or regional hemodynamics or neurohormones. Naloxone hydrochloride was also administered to anesthetized heart failure dogs. Pentobarbital anesthesia removed cortical perception of nociceptive stimulation, reduced the increase in plasma epinephrine, and abolished vasodilation in skeletal muscle that occurred in conscious dogs after naloxone hydrochloride administration but had no major effects on responses of plasma norepinephrine, systemic hemodynamics, or other regional blood flows to opiate receptor inhibition. Naloxone hydrochloride had no effect in sham-operated dogs. The results indicate that the hemodynamic effects of naloxone are mediated by an action within the central nervous system. Furthermore, since pentobarbital anesthesia did not markedly alter the hemodynamic responses to naloxone hydrochloride, the acute salutary effects of opiate receptor inhibition probably are not caused by removal of the antinociceptive effect of endogenous opioids in heart failure.

Anesthesia↗
PubMed1988

Effects of naloxone on systemic and regional hemodynamic responses to exercise in dogs.

To determine whether endogenous opiates have a role in circulatory regulation during mild to moderate exercise, 11 chronically instrumented dogs were exercised on a treadmill up a 6% incline at 2.5 and 5.0 mph, each for 20 min, after treatment with either the opiate receptor antagonist naloxone (1 mg/kg bolus and 20 micrograms.kg-1.min-1 infusion) or normal saline. Naloxone increased plasma beta-endorphin and adrenocorticotropic hormone at rest but had no effect on resting heart rate, aortic pressure, cardiac output, left ventricular time derivative of pressure (dP/dt) and ratio of dP/dt at a developed pressure of 50 mmHg and the developed pressure (dP/dt/P), or plasma catecholamines. Plasma beta-endorphin and adrenocorticotropic hormone increased during exercise. In addition, graded treadmill exercise produced proportional increases in heart rate, cardiac output, aortic pressure, left ventricular dP/dt and dP/dt/P, and blood flow to exercising muscles, right and left ventricular myocardium, and adrenal glands. However, there were no differences in the circulatory responses to exercise between animals receiving naloxone and normal saline. Thus the endogenous opiate system probably does not play an important role in regulating the systemic hemodynamic and blood flow responses to mild and moderate exercise.

Adrenocorticotropic Hormone↗
PubMed1988

Comparative effects of nitroprusside and pinacidil on myocardial blood flow and infarct size in awake dogs with acute myocardial infarction.

The effect of nitroprusside in limiting myocardial infarct was compared with that of pinacidil, a new antihypertensive agent with potent coronary vasodilator properties, in instrumented awake dogs subjected to 4 hr of left anterior descending coronary artery occlusion and 20 hr of reperfusion. Dogs were randomly assigned to receive intravenous normal saline, nitroprusside, or pinacidil beginning 40 min after the onset of coronary artery occlusion and continuing throughout the occlusion and the first hour of reperfusion. Nitroprusside and pinacidil were titrated to decrease mean aortic pressure by 25 mm Hg; normal saline had no effect on mean aortic pressure. Other systemic hemodynamic variables were not significantly altered by normal saline or nitroprusside, and myocardial blood flow did not change during normal saline infusion in normal and ischemic myocardium. In contrast, nitroprusside increased the blood flow and the endocardial/epicardial flow ratio in ischemic myocardium. This increase in ischemic myocardial blood flow was accompanied by a significant reduction in infarct size (40 +/- 3% of region at risk vs 58 +/- 4% in the normal saline group; p less than .05). Pinacidil increased heart rate, cardiac output, and the peak rate of rise of left ventricular pressure. Furthermore, despite causing a threefold to fourfold increase in normal myocardial blood flow, pinacidil had no effect on either blood flow to ischemic myocardium or infarct size (57 +/- 5%). The data indicate that the marked coronary vasodilator effect of pinacidil does not cause an increase in ischemic blood flow or a reduction in infarct size.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Short-term hemodynamic effects of vasopressin V1-receptor inhibition in chronic right-sided congestive heart failure.

Arginine vasopressin is elevated in congestive heart failure. To determine the effect of arginine vasopressin upon systemic hemodynamics and regional blood flows, we administered the specific inhibitor of the vascular action of vasopressin [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid),2-(O-methyl)-tyrosine]-arginine vasopressin [d(CH2)5Tyr(Me)AVP] to 15 dogs with chronic right-heart failure produced by tricuspid avulsion and progressive pulmonary artery constriction. The animals exhibited increased plasma arginine vasopressin and norepinephrine levels. Vasopressin inhibition increased cardiac output and left ventricular dP/dt and dP/dt/P, and it decreased total peripheral vascular resistance, whereas mean aortic pressure did not change significantly. Simultaneously, blood flow increased to skeletal muscle, kidneys, skin, and right and left ventricular myocardium. Plasma catecholamines also increased. Pretreatment with propranolol and prazosin abolished the increases in cardiac output and left ventricular function produced by vasopressin inhibition. Pretreatment also led to a decrease in mean aortic pressure after vasopressor inhibition. In contrast, administration of d(CH)2)5Tyr(Me)AVP to 11 sham-operated animals or administration of normal saline to nine sham-operated and eight heart-failure dogs was without effect either in the absence or in the presence of adrenergic receptor blockade. Thus, arginine vasopressin participates in the control of the circulation in right-sided congestive heart failure, with both a direct constrictor action on blood vessels and an indirect action by inhibition of the sympathetic nervous system.

Animals↗
PubMed1988

Double-blind comparison of butorphanol and morphine in patient-controlled analgesia.

In this study, the patient-controlled analgesia (PCA) technique was used to compare the suitability of butorphanol with that of morphine in relieving postoperative pain. Twelve patients, 19-77 years old, who had abdominal surgery, used the PCA device through the first 24-hour postoperative period. Results showed that all patients expressed satisfaction with the PCA technique. Analysis of the degree of discomfort according to the verbal description scale, recordings of respiratory rate, and assessment of sedation status showed no significant differences between patients who received butorphanol and those who received morphine. Patients were able to maintain acceptable analgesia with minimal sedation. There were no adverse side effects reported with butorphanol.

Adult↗
PubMed1987

Effects of milrinone on systemic hemodynamics and regional circulations in dogs with congestive heart failure: comparison with dobutamine.

Milrinone is a new bipyridine inotropic agent with direct vasodilator properties. To determine the role of the vasodilator action in mediating systemic and regional hemodynamic responses to milrinone, we administered two equipotent inotropic doses of either milrinone or dobutamine to dogs with chronic congestive right heart failure produced by tricuspid avulsion and pulmonary artery stenosis. Similar increases in cardiac output, right and left ventricular dP/dt, and left ventricular dP/dt/P were produced by milrinone and dobutamine; however, heart rate increased and mean aortic pressure decreased only with milrinone infusion. In addition, while total peripheral vascular resistance decreased with both agents, the decrease was greater with milrinone. Regional blood flows were measured by a radioactive microsphere method. Milrinone and dobutamine produced similar increases in myocardial blood flow and left ventricular oxygen consumption. Dobutamine infusion decreased quadriceps muscle vascular resistance and had no effect on renal and splanchnic circulations. In contrast, milrinone infusion increased vascular resistance in quadriceps muscle and decreased it in renal and splanchnic beds. Thus, when milrinone was used in inotropic doses similar to those of dobutamine, the responses in systemic and regional hemodynamics in congestive heart failure differed. Milrinone produced a greater decline in total peripheral, renal, and splanchnic vascular resistances, probably resulting from its direct vasodilator action.

Animals↗
PubMed1987

The role of endogenous opioids in congestive heart failure: effects of nalmefene on systemic and regional hemodynamics in dogs.

We studied the role of endogenous opiates and their interrelationships with the sympathetic nervous system in an experimental preparation of right-sided congestive heart failure (CHF) produced by surgical tricuspid avulsion and progressive pulmonary arterial constriction. Three groups of dogs with CHF and one group of sham-operated dogs were studied. One group of dogs with CHF was given normal saline as pretreatment, while the other two groups were pretreated with either propranolol alone (beta-blockade) or propranolol plus prazosin (alpha- plus beta-blockade). CHF was characterized by weight gain, ascites, elevated right atrial pressure, tachycardia, and reduced cardiac output. Compared with sham-operated animals, animals with CHF exhibited significantly higher baseline levels of plasma beta-endorphin and cortisol. Furthermore, only the animals with CHF responded to the opiate receptor-antagonist nalmefene with significant increases in plasma beta-endorphin, cortisol, and adrenocorticotropic hormone. Administration of nalmefene increased aortic blood pressure, cardiac output, left ventricular dP/dt and dP/dt/P, and blood flow to the myocardium, skeletal muscle, and kidneys in dogs with CHF, but had no appreciable effects in sham-operated dogs. beta-Receptor blockade abolished the increase in cardiac output, left ventricular performance, and blood flow produced by nalmefene, but had no effect on the pressor response to nalmefene. The increase in mean aortic pressure in the beta-blockade group was accompanied by an increase in skeletal muscle vascular resistance. Addition of prazosin in the alpha- plus beta-blockade group abolished the increases in mean aortic pressure and skeletal muscle vascular resistance, suggesting that the changes after propranolol probably resulted from unmasking of alpha-receptor-mediated vasoconstriction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗
PubMed1987

Systemic and regional hemodynamic effects of isomazole in awake dogs with congestive heart failure.

To determine the hemodynamic effects of isomazole, an imidazopyridine, we administered isomazole (10 and 20 micrograms/kg/min) to 10 awake dogs with right-sided congestive heart failure produced by pulmonary artery constriction and tricuspid valve avulsion. Isomazole increased cardiac output, heart rate, right ventricular and left ventricular (LV) dP/dt, LVdP/dt/P and decreased aortic pressure and total peripheral vascular resistance. Simultaneously, blood flow increased to myocardium, quadriceps muscle, brain and splanchnic beds, whereas vascular resistance decreased. Furthermore, isomazole increased LV oxygen consumption and decreased transcoronary arteriovenous oxygen difference. Similar administration of normal saline had no effects. Angiotensin II was infused to restore mean aortic pressure to base-line values during isomazole infusion; however, despite the return of aortic pressure to base-line values, cardiac output, LVdP/dt and LVdP/dt/P remained elevated. The systemic and regional hemodynamic effects of isomazole were unaffected by pretreatment with propranolol and mecamylamine. Thus, isomazole exerted positive inotropic, chronotropic and vasodilator effects in congestive heart failure dogs. The inotropic effect of isomazole was independent of the decrease in aortic pressure, and the hemodynamic effects of isomazole were not mediated via the autonomic nervous system. Furthermore, the decrease in transcoronary arteriovenous oxygen difference suggests that isomazole exerted an active coronary vasodilator action which may improve myocardial oxygen demand/supply ratio.

Angiotensin II↗
PubMed1985

What causes uptake of technetium-99m methylene diphosphonate by tumors? A case where the tumor appeared to secrete a hypercalcemia-causing substance.

A patient exhibited an unusual constellation of findings: His extraosseous lymphoma sequestered [99mTc]MDP, a bone-seeking agent, while at the same time it appeared to produce a factor that caused hypercalcemia. The dispersed lymphoma cells took up more [99mTc]MDP in vitro than did cultured lymphoblasts suggesting that the in vivo sequestration may have been, at least in part, an active intracellular process.

Cells, Cultured↗
PubMedDate not supplied

Alanine, glutamate, and ammonia exchanges in acutely ischemic swine myocardium.

Coronary artery disease causes an increase in glutamate uptake and alanine output by the heart. We assessed the effects of acute myocardial ischemia on alanine and glutamate exchange and ammonia production in 10 anesthetized open-chest domestic swine (46.9 +/- 0.7 kg). Coronary blood flow was controlled through an extracorporal perfusion circuit. After a nonischemic control period (aerobic) the blood flow in the left anterior descending coronary artery was reduced by 60%. Arterial and anterior interventricular venous samples where drawn before and during 35 min of ischemia. Subendocardial blood flow, measured using radiolabeled microspheres, decreased from 1.27 +/- 0.16 to 0.25 +/- 0.09 (ml/g)/min, and left-ventricular wall-thickening fell to 47% of aerobic values. Ischemia resulted in a significant increase in the rate of glucose uptake (p less than 0.05) and a switch to net lactate production (p less than 0.01). Ischemia did not affect the rates of alanine output (-0.9 +/- 1.0 vs. -0.3 +/- 0.3 mumol/min) or glutamate uptake (-0.4 +/- 1.1 vs. 0.3 +/- 0.6 mumol/min), but did increase the venous-arterial difference for ammonia (-4.1 +/- 4.1 to 52.7 +/- 5.5 microM, p less than 0.0001) and the ammonia output (-0.33 +/- 0.24 to 1.34 +/- 0.14 mumol/min, p less than 0.0001). In conclusion, acute ischemia did not stimulate greater alanine output or glutamate uptake. However, acute ischemia did cause an increase in anaerobic glycolysis rate and ammonia output, which reflects a profound disruption in myocardial energy metabolism.

Alanine↗
PubMedDate not supplied

Technetium 94m-labeled methoxyisobutyl isonitrile: dosimetry and resting cardiac imaging with positron emission tomography.

BACKGROUND: Development of a positron-emitting form of technetium has allowed the imaging of technetium radiopharmaceuticals with positron emission tomography (PET). We used 94mTc to compare the distribution of the myocardial perfusion agent sestamibi at rest with the conventional PET perfusion tracer 13N-labeled ammonia (13N-ammonia). METHODS AND RESULTS: Dosimetry calculations were performed with the known whole-body distribution of 99mTc-labeled sestamibi. Dynamic PET imaging of 13N-ammonia and 94mTc-labeled sestamibi (94mTc-sestamibi) for 32 minutes was performed in eight patients with previous myocardial infarction. Initial myocardial and extramyocardial distribution of 94mTc-sestamibi was compared with that of 13N-ammonia by qualitative and quantitative analysis. Quantitative comparison of the two tracers was performed with region-of-interest analysis and circumferential profiles. Qualitatively, the cardiac distribution of the tracers was similar in normal and infarcted myocardium. A decrease in the definition of the epicardial and endocardial borders of the heart was seen with 94mTc-sestamibi, presumably because of the lower dose of radionuclide injected. Quantitatively, there was no difference in infarct size, defined prospectively as tracer activity less than 20% of maximum activity for the section, between the two tracers. Circumferential profile analysis with 12-degree radial sections similarly demonstrated no difference in regional cardiac distribution of the tracers. CONCLUSIONS: These results revealed no significant difference in myocardial uptake compared with 13N-ammonia suggesting that the myocardial uptake of sestamibi correlates with that of myocardial perfusion.

Adult↗
PubMedDate not supplied

Emergency department treatment of migraine, tension, and mixed-type headache.

The complaint of headache is frequently encountered in the emergency department, but most patients with cephalalgia have a benign etiology for their pain. At least 90% of patients presenting with headache are diagnosed as suffering from benign vascular or muscle-tension (for example, migraine, tension, or mixed-type) headache. There is no consensus on the ideal therapeutic approach to these patients. Classically utilized narcotic therapy suffers from problems with efficacy, relapse, and potential for abuse and addiction. However, other agents have successively proved to be imperfect as well, despite the many therapeutic approaches that have been suggested in the medical literature. While no one drug has emerged as clearly superior for treatment of acute benign headache, recent investigations have clarified the role of certain therapies. This review is intended to familiarize emergency physicians with the latest information on most recommended therapeutic approaches to the patient with headache.

Analgesics↗
PubMedDate not supplied

The effectiveness of esophageal stethoscopy in a simulated in-flight setting.

PURPOSE: Previous research has confirmed the inability of flight nurses in an airborne BO-105 helicopter to hear breath sounds using normal or amplified transthoracic stethoscopy. The purpose of this study was to determine whether esophageal stethoscopy enabled effective auscultation of breath sounds in a simulated in-flight environment. METHODS: The cabin-sound environment of an in-flight BO-105 was recorded and recreated in an audiology laboratory, where five flight nurses were evaluated listening to taped breath sounds via an esophageal stethoscope. This audiotape model, validated in a previously published study, used a tape consisting of 24 20-second segments. Each segment, the beginning of which was marked with a beep signal, consisted of 20 seconds of silence or breath sounds. The distal (esophageal) end of the esophageal stethoscope was attached to the tape recorder; the intensity level of breath sounds heard at the stethoscope earpiece was calibrated to equate the sound level of actual esophageal breath sounds recorded on a volunteer. RESULTS: All nurses correctly identified the 24 taped segments as silent or including breath sounds 100% of the time. CONCLUSION: In the simulated environment tested, esophageal stethoscopy enabled 100% accuracy in identification of breath sounds, as compared with previously reported 0% efficacy for standard transthoracic auscultation. Study in the actual patient-care environment is indicated to confirm the usefulness of esophageal stethoscopy in the in-flight setting.

Air Ambulances↗
PubMedDate not supplied

Red cabin lights impair air medical crew performance of color-dependent tasks.

INTRODUCTION: Red cabin lighting is often used for nighttime patient transports in helicopters. This study was conducted to determine if red lighting results in impairment of color-dependent tasks. METHODS: An emergency medical services pilot adjusted red lighting in a BO-105 cabin to maximum acceptable intensity. Thirteen emergency room residents were shown positive and negative CO2 detectors and skin-colored and cyan-tinted rubber masks; percentages of correctly identified masks and detectors were noted. Subjects also read drug name and amount from 12 medication labels. Wilcoxon analysis (p = 0.05) was used to compare label reading accuracy between two groups: control (black/white lettering/background) and red (red lettering or background). RESULTS: Percentages of accurately identified masks and detectors in the red light setting were as follows: normal mask 61.5%, cyanotic mask 30.8%, negative and positive CO2 detectors 46.2%. Ability to correctly read medication labeling was significantly (p = 0.003) greater in control (76.9 +/- 10.9%) as compared to red groups (16.3 +/- 13.4%). CONCLUSION: Red cabin lighting appears to impair performance of certain critical tasks requiring color discernment. Consideration of this by medical crews working under red light conditions could reduce risk for patient-care errors.

Air Ambulances↗
PubMedDate not supplied

Can correct closed-chest compressions be performed during prehospital transport?

INTRODUCTION: The resuscitation rate from out-of-hospital cardiac arrest is low. There are many factors to be considered as contributing to this phenomenon. One factor not previously considered is the impact of a moving ambulance environment on the ability to perform closed-chest compressions. HYPOTHESIS: Proper closed-chest compressions can be performed in a moving ambulance. METHODS: A cardiopulmonary resuscitation (CPR) training mannequin with an attached skill meter (Skillmeter ResusciAnnie, Laerdal, Armonk, N.Y., USA) that measures each chest compression for proper depth and hand placement was used. Ten emergency medical technician-basic (EMT-B) certified prehospital providers were assigned into one of five teams. Each team performed a total of four sessions of five minutes of continuous closed-chest compressions on the mannequin. Two sessions were done by each team: one in the control environment with the mannequin placed on the floor, and the other in the experimental environment with the mannequin placed in the back of a moving ambulance. The ambulance was operated without warning lights and siren, and all traffic rules were obeyed. The percentage of correct closed-chest compressions was recorded for each session, and the mean values were compared using Student's t-test with alpha set at 0.01 for statistical significance. RESULTS: Ten sessions of compressions were done in both environments. The mean percentage of correct compressions was 77.6 +/- 15.6 for the control group and 45.6 +/- 18.3 for the ambulance group (p = 0.0005). CONCLUSION: A moving ambulance environment appears to impair the ability to perform closed-chest compressions.

Ambulances↗